Photo reminds us of the fattening effects of insulin

The New England Journal of Medicine recently published the photograph below. It is of a 55-year-old man with Type 1 diabetes who has been injecting insulin under the skin of his belly for more than 30 years. Those who inject insulin regularly are often advised to ‘rotate’ (vary) the site of injections. One reason for this is that if they don’t, they can run the risk of developing ‘lipohypertrophy’ – enlargement of fat cells local to where the insulin is injected. The picture below is a graphic example of this condition.

This picture, I think, serves also as a useful reminder of the potential roles that insulin has in the body. Insulin is essential to life, because without it glucose cannot be transported into the cells for fuel, and dangerously high levels of glucose can build up in the bloodstream.

However, insulin has other effects too. It is integral to fat storage, for instance. Here are three pertinent effects here:

Insulin stimulates the uptake of fat into the fat cells

Insulin activates the enzyme ‘lipoprotein lipase’ that catalyses the conversion of fat in the form of triglcyerides into smaller molecules known as fatty acids. These fatty acids, unlikely triglyceride, can make their way into the fat cells.

Insulin increases the supply of glycerol for the ‘fixing’ of fat in the fat cell

Insulin also facilitates the uptake of sugar into cells where it can be converted into glycerol In combination with fatty acids, glycerol forms triglyceride again, effectively ‘fixing’ fat in the fat cells.

Insulin inhibits breakdown and release from the fat cells

Triglyceride in the fat cells is disassembled through the action of an enzyme known as ‘hormone-sensitive lipase’. Insulin inhibits this enzyme, and therefore slows fat release from the fat cells (lipolysis).

These inherently fattening effects of insulin make it a likely key player in individuals who are struggling with their weight. More importantly, eating and living in a way which helps lower insulin levels provides the opportunity to reverse the processes listed above an facilitate fat loss.

In essence, what this means is eating a diet based on natural, unprocessed, ‘primal’ foods such as meat, fish, eggs, nuts, seeds, non-starchy vegetables and some fruit. What is notably missing from this diet are the starchy carbohydrates we’re sometimes urged to eat for their ‘essential and nutritious’ nature. The thing is, though, starchy carbs are neither essential nor especially nutritious. And the surges of insulin they tend to induce can lead us down a path to excess weight, and other health issues including cardiovascular disease, and type 2 diabetes.

12 Responses to Photo reminds us of the fattening effects of insulin

When you are being paid to develop a brain-based drug to patent for obesity, is it surprising for you suddenly the brain is the only element in the syndrome? Gosh, no. When will someone ask Guyenet where his funding comes from and what he intends to patent from his research? I would most respectfully suggest you follow his money. If a Pfizer researcher came to you to argue that statins should be in the drinking water because they will also prevent the common cold, wouldn’t you ask some tough questions before buying into that research? I’m sorry, I don’t give anyone a free pass.

As for Taubes – I know where his money comes from; his publisher. He has clearly stated that he got a 5-year-book advance. So trust me it’s to his advantage as well to keep the “debate” going because he needs to boost his books onto the best-seller lists.

Both sides benefit from the fake contention, it’s like a reality show. The actual physiology is clear – you can read nearly any medical textbook if you have doubts. Or turn and talk to the diabetics you know. It’s really simple to get yourself outta the cash-driven “debate.”

Hi John, Just wondering how your reconcile this with Stephan Guyenets posts on insulin as an antiobesity hormone? I refer to this post amongst others he has written –http://wholehealthsource.blogspot.com/2011/11/does-high-circulating-insulin-drive.html
and summarising comment that “high circulating insulin per se is neither necessary nor sufficient to cause body fat accumulation”. Surely metabolic disturbances such as insulin resistance or leptin resistance are key, not insulin alone?

Hi John,
See TWICHOO Soldiers are Down to Syringes
An Insulin level 200 times higher than normal in insulin-sensitive fat cells has a significant effect on TAG-cycling.
An Insulin level 2-ish times higher than normal in insulin-insensitive fat cells doesn’t.

Dr Briffa, what we are seeing here is not just the hypertrophy i.e. an increase in the size of fat cells, but also an increase in the number of fat cells. This phenomenon is called adipocytes proliferation. It is caused by chronic hyperinsulinemia, not just hyperinsulinemia. When insulin shoots up then goes down, that effect is not seen. For it to be seen, insulin must remain chronically high.

Another effect of chronic hyperinsulinemia is that the tissue that supplies these new fat cells with oxygen also grows bigger in a permanent fashion. So even if we could somehow reduce the size of fat cells, we still have all that associated tissue to deal with. Recent research discovered a way to deal with that associated tissue, and subsequently reduce the number of fat cells by basically starving them of oxygen and causing them to suicide. The trademark name for this new drug is Adipotide, the generic name is Prohibitin-Targeting Peptide 1.

What this means for us low carbers is that once we’ve taken care of diet, we can eventually take care of the adipocytes proliferation that occurred during all those years prior.

FrankG, i believe Leifemil’s query was regarding the whole statement/sentence with a focus on the second part (…..because without it glucose cannot be transported into the cells for fuel).
not just the first half (Insulin is essential to life) which i doubt Leifemil was disputing.

This past year my 9 yr old 90lb buff colored lab was diagnosed with diabetes. Not surprising since he eats processed dry and canned food. He ended up losing tons of weight and once we started with the insulin shots he started to finally put on weight. I wish I could afford to feed him a meat diet but it’s not possible on teachers salary. Yes insulin does put on weight and I saw it for myself with my dog.

I am answering this as a type 1 diabetic of 38 years standing. I am not a biologist or health professional so i don’t know the intricacies of every hormone interaction in the body, but I do know this. . .

The reason for weight loss in diabetics is because, as stated by someone above, insulin is vital for the movement of glucose (that all carbohydrates, of whatever type, are broken down into by the body) from the blood into cells in order to provide fuel for the body and brain to run on. Without insulin the blood becomes saturated with glucose that the body is unable to metabolise. That means that the body can’t access the nourishment it’s been fed either for energy or fat storage or anything else. Therefore, obviously, the weight falls off. But worse, that over-sweet blood causes the lethally poisonous effect of ketoacidosis. That leads to coma and death if left untreated by adding insulin, either by injection for type one or tablets to stimulate insulin production and/or control insulin resistance for type 2. (I only have limited knowledge of type 2 diabetes, but I suspect that if you get that bad injected insulin would be necessary for type 2 as well)

Obviously returning insulin levels to normal so that the body can start feeding itself and stop poisoning itself, will lead to weight gain. Back to normal that is. It doesn’t have to lead to obesity and won’t if you keep careful control of insulin/carb ratios. And calories of course.

The liver has to contain some glycogen (which is also enabled by insulin) in order to maintain correct blood glucose levels by its release when needed for energy. Without that facility you would have to continually eat when exercising. It is only when more food is eaten than is required for those two processes that the surplus is stored by the body as fat.

Insulin seems to play a part in that role too, but as I said, I don’t know the details of all the hormonal interactions during these processes. I do know that insulin is the ‘enabler’ needed for the passage of glucose between cells; many other hormones, and probably other things I know nothing about, are obviously involved as well.

In conclusion, insulin only appears to the observer to be a ‘fattening’ hormone because it allows the body to regain the weight lost before diagnosis and treatment of diabetes. And while understanding the details of how it all works is certainly fascinating, it has no relevance to the basic reality that eating more calories than the body uses leads to weight gain and vice versa. Maybe it’s not a bad idea to stop making insulin a scapegoat for weight gain in non-diabetic people as it is simply part of the whole complicated metabolic process that happens between food on the plate and fat in the body.

An afterword: type 1 diabetes is an autoimmune disease caused by the body’s immune system completely destroying the insulin producing glands in the pancreas, therefore it leaves no ability for the body to make insulin ever again and must be treated with injected insulin. Possible causes are only now beginning to be discovered and they are not dietary. It is impossible to control type 1 diabetes by diet alone, even if you live on cabbage! Insulin is vital, you cannot live without it. Type 2 is a different condition with the same result: not enough insulin (as opposed to none) to metabolise carbs. It is often, not always, caused by being overweight, can often be controlled by diet alone, but often needs medication to increase insulin production etc as stated back at the beginning. Some type 2s progress to insulin treatment.

I have realized that the wording in my previous post, in the paragraph about glycogen, is confusing. I meant it to say that insulin is necessary for the creation of stored glycogen. It is not, as that paragraph seems to imply, responsible for the release of glycogen.

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